A number of health conditions can cause or worsen tinnitus.

In many cases, an exact cause for Tinnitus is never found.



A common cause is inner ear cell damage. Tiny, delicate hairs in your inner ear move in relation to the pressure of sound waves. This triggers ear cells to release an electrical signal through a nerve from your ear (auditory nerve) to your brain. Consequently, your brain interprets these signals as sound.

If the hairs inside your inner ear are bent or broken, they can “leak” random electrical impulses to your brain, causing tinnitus.
Other causes of tinnitus include other ear problems, chronic health conditions, and injuries. Furthermore, conditions that affect the nerves in your ear or the hearing center in your brain may also contribute to the induction of tinnitus.


Clinically, subjective tinnitus is the perception of sound in the absence of auditory stimulation. In terms of neurophysiology, tinnitus is the consequence of the brain’s response to input deprivation from the auditory periphery. In the healthy auditory system, there is an ordered tonotopic frequency mapping from the auditory periphery (cochlea), through the midbrain, to the auditory cortex.

Projections in the Brain

When a region of the cochlea is damaged, the subcortical and cortical projections adjust to this chronic lack of output (plasticity). Hence, the tonotopic organization is altered. In the auditory cortex, the region that corresponds to the area of cochlear damage is termed the lesion projection zone (LPZ). After cochlear damage, neurons in the LPZ show 2 important changes: an increase in the spontaneous firing rate and an increase in the frequency representation of the neurons that border the region of damage (the so-called lesion edge frequencies).
These findings are explained in terms of a) the loss of central inhibition on the regions that are damaged and b) cortical plasticity of the neighboring regions of the cortex that are still active. As a result, tinnitus neurophysiology is related to detrimental cortical adaptation to input deprivation from the sensory periphery.